30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Levels of autolysosomal proteins in neurally derived blood exosomes distinguish patients with AD from case controls and appear to reflect the pathology of AD up to 10 years before clinical onset. 4 key findings →
Design: cross-sectional Participants: 26 Evidence: low
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Over a median follow-up of 5.1 years, 153 of 534 participants (28.7%) with prevalent or incident MCI progressed to dementia (71.3 per 1,000 person-years). 2 key findings →
Participants: 534 Evidence: moderate
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Even in a cohort of patients seen at dementia research centers, reversion from MCI was fairly common. 5 key findings →
Participants: 3,020 Evidence: moderate
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New consensus diagnostic criteria for TES were developed with a primary goal of facilitating future CTE research. 2 key findings →
Participants: 298 Evidence: low
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These findings suggest a potential vasculoprotective role of vitamin D. 2 key findings →
Design: cross-sectional Participants: 318 Evidence: low
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Aging-associated WMHs evolve significantly over a 4-year period. 5 key findings →
Design: longitudinal study Participants: 150 Evidence: moderate
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Changes in functional connectivity in DLB indicate patterns of activation that are distinct from those seen in AD and may improve discrimination of DLB from AD and cognitively normal individuals. 3 key findings →
Design: longitudinal study Participants: 88 Evidence: moderate
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There were minimal effects of lifestyle enrichment on AD biomarker trajectories (specifically rates). 5 key findings →
Design: longitudinal study Participants: 393 Evidence: moderate
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Both AD and TDP/HS contribute to hippocampal volume loss in older-old persons, with TDP/HS more strongly associated with hippocampal volume than AD in Alzheimer dementia. 3 key findings →
Design: cohort study Participants: 232 Evidence: moderate
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The FAD cortical signature appears to be similar to that described for sporadic AD. 5 key findings →
Design: longitudinal study Participants: 43 Evidence: moderate
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The data suggest that engagement in leisure activities may reduce the risk of incident dementia, possibly by providing a reserve that delays the onset of clinical manifestations of the disease. 4 key findings →
Participants: 1,772 Evidence: moderate
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We have developed MCI risk scores using variables easily assessable in the clinical setting and that may be useful in routine patient care. 2 key findings →
Design: cohort study Evidence: moderate
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With the aging US population and increasing incidence of Alzheimer disease (AD), understanding factors contributing to driving cessation among older adults is crucial for clinicians. 4 key findings →
Design: longitudinal study Participants: 283 Evidence: moderate
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Dementia-related blood biomarkers are the future of large-scale dementia risk stratification; however, the extent to which phosphorylated tau (P-tau181), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP) are associated with nonmodifiable risk factors has yet to be confirmed in the community, and the role of menopause has yet to be investigated. 4 key findings →
Design: cohort study Participants: 9,940 Evidence: moderate
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We observed 234 cases of all-cause dementia over 10 years of follow-up. 4 key findings →
Participants: 2,457 Evidence: low
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We analyzed data from 11,709 participants without a history of coronary heart disease or stroke who attended the baseline examination (1987-1989) of the prospective Atherosclerosis Risk in Communities (ARIC) study. 4 key findings →
Participants: 11,709 Evidence: moderate
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The association between patterns of physical/mental activity and dementia and how it is affected by disease susceptibility remains unknown. 4 key findings →
Design: cohort study Evidence: moderate
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< 0.001] total scores differed significantly between groups, with controls (median MoCA 28.5, 95% CI 28.0-29.0; median MMSE 30, 95% CI 30.0-30.0) outperforming prodromal (median MoCA 26, 95% CI 23.0-27.0; median MMSE 29, 95% CI 27.5-29.5) and symptomatic (median MoCA 20.5, 95% CI 17.0-24.0; median MMSE 26, 95% CI 23.5-29.0) carriers. 5 key findings →
Design: cohort study Evidence: moderate
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Of 9,361 randomized participants, 7,221 (77%) were eligible to be re-contacted. 5 key findings →
Participants: 248 Evidence: high
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We evaluated 62 Automated speech analysis demonstrated high accuracy in differentiating FTD subtypes and provided insights into the neural basis of language impairments. 3 key findings →
Design: cross-sectional Participants: 16 Evidence: moderate
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CSF biomarkers, including P-tau, T-tau, Aβ 42 , Aβ 40 , and NFL, support in vivo identification of AD neuropathology and correlate with FTLD neuropathology. 4 key findings →
Participants: 101 Evidence: low
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Although all p-tau variants increased across the AD continuum, p-tau217 Lilly showed the greatest dynamic range (13-fold increase vs 1.9-5.4-fold increase for other p-tau variants for AD dementia vs non-AD). 2 key findings →
Participants: 334 Evidence: low
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We developed, replicated, and validated an MRI measure of cerebrovascular and neurodegenerative pathologies that are associated with clinical and neuropathologic diagnosis of AD and related to established biomarkers. 5 key findings →
Design: cross-sectional Participants: 1,175 Evidence: moderate
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Our results indicate that APOE ε4 is independently associated with a greater severity of LB pathology. 5 key findings →
Design: case-control study Evidence: moderate
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Regions with Z -scores Results Patients with AD (n = 206) had a median of 12 outlier regions (out of a possible 148), with the highest proportion of outliers (47%) in the parahippocampal gyrus. 2 key findings →
Participants: 33,072 Evidence: low
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Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled.
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 30,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,037 records (3.4% of the library) are not peer-reviewed — 964 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →